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V Sankar

Publications and source records attributed to V Sankar.

7 recordsLinked to original sources
PubMed2001

Publication rates of scientific papers presented at the Otorhinolarygological Research Society meetings.

The aim of this study was to determine the publication rate of scientific papers in peer review journals presented at the Otorhinolarygological Research Society (ORS) meetings from 1978 to 1995 inclusive. The abstracts of the presentations at ORS meetings are published in Clinical Otolaryngology. A MEDLINE search was performed on abstracts presented at ORS meetings from 1978 to 1995 using both authors and key words within the text of the abstract. The publication rate, journal of publication, time to publication, change in contents, change in authors and change in conclusions of abstracts were tabulated. The publication rate for papers presented at ORS meetings from 1978 to 1995 was 69.09%. The average time to publication was 22.5 months. Papers derived from the ORS abstracts were most commonly published in Clinical Otolaryngology (34%) and Journal of Laryngology and Otology (18.64%). The results indicate that nearly 69% of presented material at the biannual ORS meetings eventually get published in peer reviewed journals. This compares favourably with publication rate of other specialities.

Bibliometrics↗
PubMed2001

Oral manifestations in patients with aplastic anemia.

OBJECTIVE: The aim of the present study was to characterize the prevalence and risks of oral complications in aplastic anemia (AA). STUDY DESIGN: Approximately 79 patients with AA (age, 37 +/- 17 years) and 66 control patients with schizophrenia (age, 33 +/- 12 years) were examined. Records were reviewed for demographic, clinical, and radiographic information. Prior medical therapy, laboratory values, disease duration, and medical treatment response were noted for patients with AA. Odds ratios (OR) and 95% CI were calculated for oral manifestations in cases and in control subjects. Univariate analysis identified important variables for logistic regression. RESULTS: Patients with AA presented more frequently with oral petechiae (OR = 49; 95% CI, 2.9-825), gingival hyperplasia (OR = 27; 95% CI, 1.6-463.5), spontaneous gingival bleeding (OR = 27; 95% CI, 1.6-463.5), and herpetic lesions (OR = 27; 95% CI, 1.6-463.5). Prior cyclosporine use was associated with gingival hyperplasia (P =.0001). No other predictors for oral manifestations or treatment outcomes were found. CONCLUSIONS: Oral soft tissue changes and infections were more common in patients with AA. Prior cyclosporine use was predictive of the presence of gingival hyperplasia.

Adult↗
PubMed2001

Recovery of locomotor function in adult paraplegic frogs by inductive lability in the distal isolated spinal cord neural networks.

We postulated (Krishnan, 1991) that in a spinal cord transected adult paraplegic mammal locomotor functions can be revived if polyneuronal innervation is reinduced in the paralyzed hind limb muscles. This procedure destabilizes the neural networks and induces new synaptic growth in the distal isolated cord. In this pilot project we tested the hypothesis in cord-transected adult paraplegic frogs. Polyneuronal innervation was reinduced by crushing the sciatic nerve in the right upper thigh. Left limb sciatic nerve was not crushed and served as control. Another group of adult frogs had only cord transection without nerve crush. Five to seven weeks postnerve crush, full powered flexion-extension movements in the hip and knee joints appeared in the right hind limb and were used for swimming and surface progression. Movements gradually declined over the next weeks, which in some animals was seen preserved even beyond 120 days. Paraplegic frogs without nerve crush did not show any recovery of locomotor function. Interestingly, the uncrushed contralateral limb also produced transient, weak locomotor-like movements. This lasted for 4 to 6 days and waned out completely thereafter. These results validate our hypothesis on methods to generate new synaptic sprouts and reconnections to redrive the locomotor system. We had recommended earlier that destabilization procedure should be included as an essential component in treatment strategies for spinal cord injury repair for effective relinking of the severed cord ends.

Animals↗
PubMed2001

Spinal cord injury repair research: a new combination treatment strategy.

The optimism that a cure will soon be found for paraplegia and quadriplegia is strongly founded on the series of discoveries in the last two decades which showed that adult mammalian spinal cord axons can be made to regenerate given appropriate conditions and microenvironment. But then, why no cure yet in sight? Why is the delay? Spinal cord scientists are encountering a newfound obstacle in regeneration research. While axons do regenerate up and down through a graft/transplant placed at the injury site, they fail to regenerate further on once they reach healthy cord tissue beyond the injury zone. Research from our laboratory since the 1980s found that the principal reason for this failure of long distance regeneration is that the neural circuitry these axons have to traverse through are in a well-stabilized state which is unreceptive and refractory to new growth. Successful long distance regeneration is possible only within labilized (destabilized) neural tissues. We have shown simple and reliable methods of inducing labile state in adult spinal cord neural circuitry. This is achieved by inducing polyneuronal spinal motor control in the paralyzed limb muscles. We had predicted (Krishnan, 1991, 1983) two outcomes of inductive lability in paraplegia. One is partial revival of functions in the paralyzed limbs. The second outcome addresses effective relinking of the severed cord ends. Our preliminary results from adult paraplegic frogs convince us that inductive lability in these animals is capable of generating new growth and new connections in the distal isolated cord. Locomotor rhythm and function reappeared in the hind limbs, which enabled these animals to swim and progress on surface for long periods of observation up to 120 days. Based on these results we now recommend that inductive lability should be included as an essential component in the treatment strategy for spinal cord injury repair for effective relinking of the severed cord ends.

Animals↗
PubMedDate not supplied

Cationic liposome-mediated gene transfer to rat salivary epithelial cells in vitro and in vivo.

BACKGROUND: Previously we have shown that gene transfer to salivary gland epithelial cells readily occurs via recombinant adenoviruses, although the response is short-lived and results in a potent host immune response. The aim of the present study was to assess the feasibility of using cationic liposomes to mediate gene transfer to rat salivary cells in vitro and in vivo. METHODS: Initially, for transfection in vitro, we used two cationic liposome formulations (GAP-DLRIE/DOPE and DOSPA/DOPE) complexed with plasmid encoding human growth hormone (hGH) as a reporter gene. Thereafter, using GAP-DLRIE/DOPE, plasmids were transferred to rat salivary glands in vivo, and hGH levels measured in saliva, serum and gland extracts. RESULTS: Under optimal conditions, transfection of rat submandibular glands (SMGs) was consistently observed. Approximately 95% of the cells transfected with a plasmid encoding beta-galactosidase were acinar cells. Maximal hGH expression was obtained during the first 48 h post-transfection using a plasmid encoding the hGH cDNA and complexed with GAP-DLRIE/DOPE. hGH was detected in gland extracts and saliva, and occasionally in serum. No systemic or local gland pathology was consistently or significantly observed. CONCLUSIONS: The levels of the reporter gene product, hGH, obtained after GAP-DLRIE/DOPE-mediated gene transfer are considerably lower (<0.5%) than those achieved with adenoviral vectors (10(8) PFU). Nonetheless, cationic liposome-mediated gene transfer to salivary glands may be useful for potential therapeutic applications.

Amylases↗